PuSH - Publication Server of Helmholtz Zentrum München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Kulig, P.* ; Musiol, S. ; Freiberger, S.N.* ; Schreiner, B.* ; Gyulveszi, G.* ; Russo, G.* ; Pantelyushin, S.* ; Kishihara, K.* ; Alessandrini, F. ; Kundig, T.* ; Sallusto, F.* ; Hofbauer, G.F.L.* ; Haak, S. ; Becher, B.*

IL-12 protects from psoriasiform skin inflammation.

Nat. Commun. 7:13466 (2016)
Publ. Version/Full Text Research data DOI
Open Access Gold
Creative Commons Lizenzvertrag
Neutralization of the common p40-subunit of IL-12/23 in psoriasis patients has led to a breakthrough in the management of moderate to severe disease. Aside from neutralizing IL-23, which is thought to be responsible for the curative effect, anti-p40 therapy also interferes with IL-12 signalling and type 1 immunity. Here we dissect the individual contribution of these two cytokines to the formation of psoriatic lesions and understand the effect of therapeutic co-targeting of IL-12 and IL-23 in psoriasis. Using a preclinical model for psoriatic plaque formation we show that IL-12, in contrast to IL-23, has a regulatory function by restraining the invasion of an IL-17-committed gdT (gdT17) cell subset. We discover that IL-12 receptor signalling in keratinocytes initiates a protective transcriptional programme that limits skin inflammation, suggesting that collateral targeting of IL-12 by anti-p40 monoclonal antibodies is counterproductive in the therapy of psoriasis.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
11.329
2.922
72
72
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Scientific Article
Keywords Delta T-cells; Interleukin-12/23 Monoclonal-antibody; Chronic Plaque Psoriasis; Necrosis-factor-alpha; Gamma-delta; Interferon-gamma; Epidermal-keratinocytes; Increased Expression; Gene-expression; Cutting Edge
Language english
Publication Year 2016
HGF-reported in Year 2016
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Journal Nature Communications
Quellenangaben Volume: 7, Issue: , Pages: , Article Number: 13466 Supplement: ,
Publisher Nature Publishing Group
Publishing Place London
Reviewing status Peer reviewed
Institute(s) Institute for Allergy Research (IAF)
POF-Topic(s) 30202 - Environmental Health
Research field(s) Allergy
PSP Element(s) G-505400-004
DOI 10.1038/ncomms13466
WOS ID WOS:000389038800001
Erfassungsdatum 2016-12-31
[➜Report correction]